Arteriosclerotic lesions are found in the coronary arteries of spawning Pacific Salmon (Oncorhynchus) and steelhead trout. The latter, unlike Pacific salmon, may survive the spawning act and their arterial lesions are reversible. Spawning and post-spawning salmon have a profound abnormality in theri blood coagulation mechanism which has been attributed by the P.I. to disseminated intravascular thrombosis or clotting (DIC). It is possible that the arterial lesions might represent small thrombi which become covered over by endothelial cells and then are incorporated into the intima. Focal necrotic lesions are found in the gills of these fish and it has been suggested that these are embolic in nature. Are these lesions and those in the coronary arteries related in any way to the coagulation abnormalities? Raising the temperature even a few degrees produces marked shortening of prothrombin and partial thromboplastin times in salmon and these findings are far more striking than any of the changes of 'hypercoagulability' seen in women on the pill. Will 'hypercoagulability' if defined as acceleration of the in vitro clotting time, predispose to thrombosis and result in arterial lesions? We hope to obtain answers to some of these questions by a careful gross, electron and light microscopic examination of the organs and tissues of spawning and post-spawning salmon. We will carefully search for evidence of thromboembolic disease with particular attention to the lesions in the gills and the evolution of the arteriosclerotic lesions in the coronary arteries. Using the above techniques we will also study the lesions in salmon or steelhead that may occur in 'hypercoagulability' induced either by raising the temperature in salmon or on the infusion of serum. If a relationship between 'hypercoagulability' and arteriosclerosis is established, this would supply the first good experimental support to the old Rokitansky-Duguid encrustation theory of atherosclerosis.